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  1. Apr 2020
    1. . Obesity, insulin resistance, hyperglycemia, and diabetic renal failure contribute significantly and independently to the impaired wound healing observed in diabetics
    2. Steroids used after the first 3 to 4 days after injury do not affect wound healing as severely as when they are used in the immediate postoperative period.
    3. The major effect of steroids is to inhibit the inflammatory phase of wound healing (angiogenesis, neutrophil and macrophage migration, and fibroblast proliferation) and the release of lysosomal enzymes
    4. Large doses or chronic usage of glucocorticoids reduce collagen synthesis and wound strength
    5. Mild to moderate normovolemic anemia does not appear to adversely affect wound oxygen tension and collagen synthesis. However, profound anemia with 15% less hematocrit can interfere with wound healing
    6. The level of vasoconstriction of the subcutaneous capillary bed is exquisitely responsive to fluid status, temperature, and hyperactive sympathetic tone as is often induced by postoperative pain. Correction of these factors can have a remarkable influence on wound outcome, particularly on decreasing wound infection rates
    7. Surgically closed wounds need mostly epithelialization for healing
    8. while open wounds require a combination of tissue contraction, connective tissue deposition, and epithelialization to a lesser extent. Chronic ulcers heal by secondary intention similar to open wounds.
    9. Wounds with delayed healing are characterized by decreased wound-breaking strength in comparison to wounds that heal at a normal rate; however, they eventually achieve the same integrity and strength as wounds that heal normally.
    10. Delayed primary closure, or healing by tertiary intention, represents a combination of the first two, consisting of the placement of sutures, allowing the wound to stay open for a few days, and the subsequent closure of the sutures
    11. Surgical wounds can heal in several ways. An incised wound that is clean and closed by sutures is said to heal by primary intention
    12. Often, because of bacterial contamination or tissue loss, a wound will be left open to heal by granulation tissue formation and contraction; this constitutes healing by secondary intention
    13. By definition, an acute wound becomes chronic if healing is not achieved after 4 weeks of treatment.
    14. An effective therapy to combat biofilm should include effective removal of the biofilm, antimicrobial eradication of bacteria/organisms, and prevention of biofilm recurrence, and these treatment options may need to be repeated multiple times to achieve effective therapy.
    15. A few products have been suggested to control and remove biofilms, such as surfactant and some wound cleansing formulas. In addition, topical broad-spectrum antimicrobials such as silver, iodine, honey, and others have been suggested to aid in the treatment of biofilms.
    16. The best method of treating wounds with biofilms is not well defined. It is believed that frequent debridement to mechanically remove the biofilm remains to be the best method of treatment. The frequency of debridement is not well defined, although a weekly debridement has been suggested to improve healing. More than one method of debridement might be needed in wounds resistant to healing.
    17. The host responds to the biofilms by mobilizing macrophages and neutrophils to the biofilm area, resulting in secretions of high levels of reactive oxygen species and proteases that can cause damage to the normal and healing tissue. The resulting increase in exudate production provides a source of nutrients to the biofilms, leading to more resistance to healing.
    18. The presence of biofilms leads to delayed wound healing by stimulating chronic inflammation in the wound.
    19. Furthermore, it rapidly recovers form mechanical disruption, such as debridement, within 24 hours
    20. Bacterial species develops the extracellular polymeric substances (EPS) and resistance to disinfectants, antiseptics, and antibiotics in 6 to 12 hours. The biofilm then develops into mature colonies in 2 to 4 days
    21. In some cases, the biofilm allows bacteria to become quiescent and thus become less sensitive to antimicrobials that typically affect dividing bacterial cells.
    22. The genetic plurality is passed horizontally among bacteria in the wound, adding to the resistance to treatment and allowing the bacteria to avoid the defense mechanisms of the host such as bacterial phagocytosis, neutrophil degranulation, and formation of reactive oxygen species.
    23. Bacteria will then begin to exhibit phenotypic and genotypic plurality: the former allows bacteria to adapt to different growth conditions such as nutrient availability, pH, and oxidizing potential within the biofilm, while the latter allows for virulence and bacterial resistance to drugs.
    24. The presence of biofilms protects bacteria from the host defenses.
    25. Once a biofilm colony forms, it will continuously shed bacteria to uncolonized areas, causing more biofilm colonies to form.
    26. Lastly, in the third stage, organisms secrete a surrounding protective matrix called the extracellular polymeric substance (EPS).
    27. This stage depends on a microbial-to-microbial cell communication system, called quorum sensing, in which small signaling molecules are released and gradually increase in concentration. The signaling molecules regulate gene expression and help form the biofilm.
    28. This stage depends on a microbial-to-microbial cell communication system, called quorum sensing, in which small signaling molecules are released and gradually increase in concentration.
    29. The second stage is the permanent adhesion or maturation stage in which the organisms permanently attach, proliferate, and maturate in the wound surface.
    30. Biofilms are formed in three stages. The first stage—the reversible bacterial adhesion stage—is formed by adhesion of bacteria to the surface of the wound
    31. Biofilm is the term used for the bacterial growth on a chronic wound that is encapsulated by a protective layer made up of the host and bacterial proteins. Bjarnsholt et al have suggested a simplified definition of the biofilm as “an aggregate of bacteria tolerant to treatment and the host defense.”
    32. Biofilms lead to a chronic inflammatory process that will interfere with healing
    33. Chronic wounds, in general, behave differently in relation to bacterial growth when compared to acute wounds. Chronic wounds develop bacterial growth that is resistant to invasion by antibiotics and is protected from the host immune defenses.
    34. In addition, HBOT was found to reduce mortality rates from necrotizing fasciitis, and significantly decreased wound size in nonhealing diabetic wounds.
    35. HBOT was found to have improved amputation rates in patients with gas gangrene with better healing.
    36. HBOT was found to improve graft survival, complete healing of grafts, and lessen infection in patients with a graft. Patients with osteoradionecrosis showed improved bone changes.
    37. HBOT was found to improve graft survival, complete healing of grafts, and lessen infection in patients with a graft
    38. Although there are numerous indications and potential indications for HBOT, there are 14 accepted indications by Undersea and Hyperbaric Medical Society, and the FDA. Indications related to wounds and ulcers include clostridial myonecrosis, crush injury, radiation-induced soft tissue and bone necrosis, necrotizing soft tissue infections, diabetic ulcers Wagner III or higher, refractory osteomyelitis, and thermal burns.
    39. The therapeutic pressure should be at least 1.4 ATA.
    40. The Undersea and Hyperbaric Medical Society (UHMS) defined HBOT as an intervention that involves breathing near 100% oxygen intermittently under high pressure achieved by a pressurized chamber to more than sea level pressure (sea level pressure = 1 atmosphere absolute [ATA]).
    41. systemic therapy included supplemental inspired oxygen therapy and pressurized oxygen treatment
    42. Chronic wounds have a decreased oxygen supply, and for a long time lack of oxygen was recognized as a potential cause of delayed healing.
    43. Oxygen is required for almost all steps of wound healing and is also an important factor in the body’s defense against bacterial infection
    44. In addition to its role in healing, oxygen plays an essential role in the production of reactive oxygen species such as superoxide that are angiogenesis stimulators and are bacteriostatic
    45. At present, only platelet-derived growth factor BB (PDGF-BB) is currently approved by the FDA for treatment of diabetic foot ulcers. Application of recombinant human PDGF-BB in a gel suspension to these wounds increases the incidence of total healing and decreases healing time.
    46. Recombinant molecular biologic means permit the purification of high concentrations of individual growth factors
    47. Disappointingly, a recent meta-analysis failed to demonstrate any value for autologous platelet-rich plasma in the treatment of chronic wounds
    48. This approach allows treatment with patient-specific factors at an apparently physiologic ratio of growth factor concentrations.
    49. Autologous growth factors are harvested from the patient’s own platelets, yielding an unpredictable combination and concentration of factors, which are then applied to the wound.
    50. Bioengineered skin substitutes have evolved from keratinocyte monolayers to dermal equivalents to split-thickness products with a pseudo-epidermis, and most recently, to products containing both epidermal and dermal components that resemble the three-dimensional structure and function of normal skin (see Table 9-11). Indicated for use with standard compression therapy in the treatment of venous insufficiency ulcers and for the treatment of neuropathic diabetic foot ulcers, these bilayered skin equivalents also are being used in a variety of wound care settings.
    51. Fibroblasts stimulated by growth factors can produce type I collagen and glycosaminoglycans (e.g., chondroitin sulfates), which adhere to the wound surface to permit epithelial cell migration, as well as adhesive ligands (e.g., the matrix protein fibronectin), which promote cell adhesion.
    52. Viable fibroblasts can be grown on bioabsorbable or nonbioabsorbable meshes to yield living dermal tissue that can act as a scaffold for epidermal growth.
    53. CEAs are available from cadavers, unrelated adult donors, or neonatal foreskins.
    54. Until the epithelial sheets are sufficiently expanded, the wound must be covered with an occlusive dressing or a temporary allograft or xenograft.
    55. Their disadvantages include limited survival, high cost, and the need for multiple applications (Table 9-10). Allografting, albeit with a very thin graft, may at times be required to accomplish complete coverage.

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    1. cute coronary syndrome (ACS)4/81(4.94%)
    2. Malignant arrhythmia2/81(2.47%)
    3. Patients presented with functional damage involving multiple vital organs, including respiratory failure (80 [94.1%]), shock (69 [81.2%]), ARDS (63 [74.1%]) arrhythmia (51 [60.0%]), acute myocardial injury (38 [44.7%]), acute liver injury (30 [35.3%]) and sepsis (28 [32.9%]) (Table 5)
    4. Most patients had abnormal myocardial zymograms characterized by increased creatine kinase in 31 (36.5%) and increased lactate dehydrogenase in 70 (82.4%) patients.
    5. The most common cause of death in 81 of the 85 patients was respiratory failure (38, 46.91%), followed by septic shock (16, 19.75%), multiple organ failure (13, 16.05%) and cardiac arrest (7, 8.64%).
    1. In >95% of patients who survive to reach the ED, the BAI occurs just distal to the left subclavian artery, where it is tethered by the ligamentum arteriosum (Fig. 7-24). In 2% to 5% of patients the injury occurs in the ascending aorta, in the transverse arch, or at the diaphragm
    2. Posterior rib fractures, sternal fractures with laceration of small vessels, and mediastinal venous bleeding also can produce similar hematomas.
    3. As with neck injuries, hemodynamically stable patients with transmediastinal gunshot wounds should undergo CT scanning to determine the path of the bullet
    4. Patients at risk for an esophageal injury should undergo bedside esophagoscopy or soluble contrast esophagography followed by barium examination to look for extravasation of contrast
    5. For penetrating thoracic trauma, physical examination, plain posteroanterior and lateral chest radiographs with metallic markings of wounds, and pericardial ultrasound will identify the majority of injuries.44 Injuries of the esophagus and trachea are the exceptions.
    6. The mediastinal abnormality may suggest the location of the arterial injury (i.e., left-sided hematomas are associated with descending blunt aortic injuries [BAI], whereas right-sided hematomas are seen with innominate injuries)
    7. Widening of the mediastinum on initial anteroposterior chest radiograph, caused by a hematoma around an injured vessel that is contained by the mediastinal pleura, suggests an injury of the great vessels.
    8. Occult thoracic vascular injury must be diligently sought due to the high mortality of a missed lesion.
    9. Pneumomediastinum following blunt trauma that is identified on CT imaging is a poor predictor of aerodigestive injury; selective workup is appropriate
    10. a persistent hemothorax that is not drained by two chest tubes is termed a caked hemothorax and mandates immediate thoracotomy
    11. Patients with hemothorax must have a chest radiograph documenting complete evacuation of the chest
    12. Patients with persistent pneumothorax, large air leaks after tube thoracostomy, or difficulty ventilating should undergo fiber-optic bronchoscopy to exclude a tracheobronchial injury or presence of a foreign body.
    13. Although immediate needle thoracostomy decompression with a 14-gauge angiocatheter may be indicated in the field, tube thoracostomy in the midaxillary line should be performed immediately in the ED before a chest radiograph is obtained (Fig. 7-3). Recent studies suggest that preferred location for needle decompression may be the fifth intercostal space in the anterior axillary line due to body habitus.

      needle thoracostomy (5th intercostal ant axil) tube thoracostomy CXR

    14. In cases of tension pneumothorax, the parenchymal tear in the lung acts as a one-way valve, with each inhalation allowing additional air to accumulate in the pleural space. The normally negative intrapleural pressure becomes positive, which depresses the ipsilateral hemidiaphragm and shifts the mediastinal structures into the contralateral chest. Subsequently, the contralateral lung is compressed and the heart rotates about the superior and inferior vena cava; this decreases venous return and ultimately cardiac output, which culminates in cardiovascular collapse.
    15. Tension pneumothorax and simple pneumothorax have similar signs, symptoms, and examination findings, but hypotension qualifies the pneumothorax as a tension pneumothorax.
    16. If the trachea is completely transected, a nonpenetrating clamp should be placed on the distal aspect to prevent tracheal retraction into the mediastinum; this is particularly important before placement of the endotracheal tube.
    17. If the chest tube output is initially 20% of the patient’s blood volume (80 mL/kg) or is persistently >1 to 2 mL/kg per hour, thoracotomy should be considered.
    18. Persistent hemorrhage from a chest tube after blunt trauma most often is due to injured intercostal arteries; for unusual persistent bleeding
    19. In patients with peripheral bronchial injuries, indicated by persistent air leaks from the chest tube and documented by endoscopy, bronchoscopically directed fibrin glue sealing may be useful.
    20. Bronchoscopy should be performed to evaluate the trachea in patients with a persistent air leak from the chest tube or mediastinal air.
    21. In patients with clear indications for operation, essential radiographs should be taken, and the patient should be transported to the OR immediately. Such patients include those with blunt trauma and massive hemothorax, those with penetrating trauma and an initial chest tube output of >1 L, and those with abdominal trauma and ultrasound evidence of extensive hemoperitoneum.
    22. During diagnostic evaluation, type O RBCs (O-negative for women of childbearing age) and thawed AB plasma should be administered at a ratio of 2:1. Type-specific RBCs should be administered as soon as available.
    23. Definitive treatment is closure of the chest wall defect and tube thoracostomy remote from the wound.
    24. Temporary management of this injury includes covering the wound with an occlusive dressing that is taped on three sides. This acts as a flutter valve, permitting effective ventilation on inspiration while allowing accumulated air to escape from the pleural space on the untapped side, so that a tension pneumothorax is prevented.
    25. Complete occlusion of the chest wall defect without a tube thoracostomy may convert an open pneumothorax to a tension pneumothorax.
    26. Because complete typing and cross-matching takes up to 45 minutes, patients requiring emergent transfusions are given type O-negative RBCs.

      Emergent patients are given O blood group

    27. In either scenario, a massive hemothorax is an indication for operative intervention, but tube thoracostomy is critical to facilitate lung reexpansion, which may improve oxygenation and cardiac performance as well as tamponade venous bleeding.

      improving oxygenation cardiac performance tamponade venous bleeding

    28. After blunt trauma, a hemothorax is usually due to multiple rib fractures with severed intercostal vessels, but occasionally bleeding is from lacerated lung parenchyma, which is usually associated with an air leak
    29. Although it may be estimated on chest radiograph, tube thoracostomy is the only reliable means to quantify the amount of hemothorax.
    30. Temporary control of hemorrhage, and at times definitive repair, may be accomplished with skin staples for left ventricular lacerations; the myocardial edges of the laceration must coapt in diastole for stapling to be technically feasible.

      skin staples for left ventricular lacerations as bleeding corntrol or repair is used.myocardial edges should coapt during diastole.

    31. Before repair of the injury is attempted, hemorrhage should be controlled; injuries to the atria can be clamped with a Satinsky vascular clamp, whereas digital pressure is used to occlude the majority of ventricular wounds. Foley catheter occlusion of larger stellate lesions is described, but even minimal traction may enlarge the original injury.

      bleeding control is first. satinsky clamp can be used for atria inj but for ventricular, mostly digital pressure is used. minimal stretch may enlarge inj (Foley)

    32. Endovascular stenting is now the mainstay of treatment.98,99 While endograft sizing has improved, the major question is long-term outcome in younger patients. Open repair of the descending aorta is accomplished using partial left heart bypass to prevent spinal cord and splanchnic ischemia and reduce left ventricular afterload (Fig. 7-57).100 Nonoperative management for grade I intimal aortic injuries is accomplished with antiplatelet agents and blood pressure control.

      mainsty is endovascular stenting. but what is the long term outcome for younger patient with improved endograft sizing? partial left hear bypass for descending aorta repair is to spinal cord and splanchnic ischemia prevention and afterload of left ventricle reduction. antiplatelet and blood pressure control for grade I intimal aortic inj is used.

    33. Descending BAI may require urgent intervention. However, operative intervention for intracranial or intra-abdominal hemorrhage or unstable pelvic fractures takes precedence. To prevent aortic rupture, pharmacologic therapy with a selective β1-antagonist, esmolol, should be instituted in the trauma bay, with a target SBP of <100 mmHg and heart rate of <100/min.

      op intervention intracranial/abdominal or unstable pelvic fx overweigh descending BAI that may require urgent intervention. β1-antagonist, esmolol, is used for aortic rupture prevention (SBP<100 mmHg, HR<100/min goal)

    34. Subclavian artery injuries can be repaired using lateral arteriorrhaphy or PTFE graft interposition; due to its multiple branches and tethering of the artery, end-to-end primary anastomosis is not advocated if there is a significant segmental loss.

      PTFE graft or lateral arteriorrhaphy is suitable for subclavian art inj; but end-to-end primary anastomosis despite significant segmental loss is not recommended due to multiple braching.

    35. Innominate artery injuries are repaired using the bypass exclusion technique,96 which avoids the need for cardiopulmonary bypass. Bypass grafting from the proximal aorta to the distal innominate with a prosthetic tube graft is performed before the postinjury hematoma is entered. The PTFE graft is anastomosed end-to-side from the proximal undamaged aorta and anastomosed end-to-end to the innominate artery (Fig. 7-56). The origin of the innominate is then oversewn at its base to exclude the pseudoaneurysm or other injury.

      bypass exclusion is useful for innominate art inj which include; before postinjury enterance of hematoma, bypass grafting the distal innominate with proximal aorta. end-to-side grafting with PTFE from proximal undamaged aorta and end-to-end to the innominate art. then oversewing the origin of innominate to exluding of psedoaneurism and...

    36. The most common injuries from both blunt and penetrating thoracic trauma are hemothorax and pneumothorax. More than 85% of patients can be definitively treated with a chest tube. The indications for thoracotomy include significant initial or ongoing hemorrhage from the tube thoracostomy and specific imaging-identified diagnoses (Table 7-10). One caveat concerns the patient who presents after a delay. Even when the initial chest tube output is 1.5 L, if the output ceases and the lung is reexpanded, the patient may be managed nonoperatively if hemodynamically stable.

      chest tube can treat 85% of hemo/pneumothoraxes, if significant bleeding from tube thoracostomy initially or ongoing was present, thoracotomy is indicated. patient delayed presentation is a caveat. nonop manageing is possible in stable patient with ceased output and rexpanded lungs even after 1.5 L output.

    37. After debridement of devitalized tissue, tracheal injuries are repaired end-to-end using a single layer of interrupted absorbable sutures. Associated injuries of the esophagus are common in penetrating injuries due to its close proximity. After debridement and repair, vascularized tissue is interposed between the repaired esophagus and trachea, and a closed suction drain is placed. The sternocleidomastoid muscle or strap muscles are useful for interposition and help prevent postoperative fistulas.

      end-to-end repair of tracheal damages with absorbale sutures after debridement. then placing vascularized tissue between repaired esophagus and trachea and close drain. SCM and strap mus are useful for interposition and fistula prevention.

    38. Fractures of the larynx and trachea may manifest as cervical emphysema. Fractures documented by CT scan are usually repaired. Common injuries include thyroid cartilage fractures, rupture of the thyroepiglottic ligament, disruption of the arytenoids or vocal cord tears, and cricoid fractures.

      larynx and trachea fx can result cervical emphysema, usually thyroid cartilage, thyroepiglottic lig rupture, arytenoid or vocal cord damage and cricoid fx,

    39. Thrombosis of the internal jugular veins caused by blunt trauma can occur unilaterally or bilaterally and is often discovered incidentally because most patients are asymptomatic. Bilateral thrombosis can aggravate cerebral edema in patients with serious head injuries; stent placement should be considered in such patients if ICP remains elevated.

      blunt trauma can cause thrombosis of int jugular veins asymptotically, can cause cerebral edema if bilateral in serious head inj, and if ICP remained elevated stenting should be considered

    40. The role of carotid stenting for grade II or III internal carotid artery injuries remain controversial; current literature suggests stenting be reserved for symptomatic patients or markedly enlarging pseudoaneurysms.

      for symptomatic patients and markedly enlarging pseudoaneurysms, stenting is suggested

    41. Because treatment must be instituted during the latent period between injury and onset of neurologic sequelae, diagnostic imaging is performed based on identified risk factors (Fig. 7-55).91 After identification of an injury, antithrombotics are administered if the patient does not have contraindications (intracranial hemorrhage, falling hemoglobin level with solid organ injury or complex pelvic fractures). Heparin, started without a loading dose at 15 units/kg per hour, is titrated to achieve a PTT between 40 and 50 seconds or antiplatelet agents are initiated (aspirin 325 mg/d or clopidogrel 75 mg/d). The types of antithrombotic treatment appear equivalent in published studies to date, and the duration of treatment is empirically recommended to be 6 months.

      diagnostic imaging before onset of neurologic complications while taking

    42. Early recognition and management of these injuries is paramount because patients treated with antithrombotics have a stroke rate of <1% compared with stroke rates of 20% in untreated patients.

      antithrombotics for blunt inj of carotid and vertebral art decreases stroke rates from 20 to 1%

    43. Vertebral artery injuries due to penetrating trauma are difficult to control operatively because of the artery’s protected location within the foramen transversarium. Although exposure from an anterior approach can be accomplished by removing the anterior elements of the bony canal and the tough fascia covering the artery between the elements, typically the most efficacious control of such injuries is angioembolization. Fogarty catheter balloon occlusion, however, is useful for controlling acute bleeding if encountered during neck exploration.

      penetrating traumatic vertebral art inj are better controled by angioembolization, rather than removal of ant of foramen transversarium. and Fogarty catheter baloon occlusion for acute bleeding while exploring.

    44. Tangential wounds of the internal jugular vein should be repaired by lateral venorrhaphy, but extensive wounds are efficiently addressed by ligation. However, it is not advisable to ligate both jugular veins due to potential intracranial hypertension.

      for tangential inj of int jugular vein lateral vonorrhaphy is used and for extensive damages, ligation, but not bilaterally to preventing IC HTN.

    45. Otherwise, carotid shunting should be done selectively as in elective carotid endarterectomy, but the patient should be systemically anticoagulated. Currently, we administer heparin with an ACT target of 250 sec.

      in elective endarterectomy doing carotid shunt should be considered after getting systemically antigoagulation with heparinn for 250 sec ACT goal

    46. Prompt revascularization of the internal carotid artery, using a temporary Pruitt-Inahara shunt, should be considered in patients arriving in profound shock.

      in profound shock, using Pruitt-Inahara shunt for revascularization of int carotid art is considered

    47. All carotid injuries should be repaired except in patients who present in coma with a delay in transport.

      comatose patient with transporting delay should not get carotid repair contrary to other carotid inj

    48. approximately 3% of patients who present with flaccid quadriplegia have concussive injuries, and these patients represent the very few who seem to have miraculous recoveries.

      concussive inj resulting flaccid quadriplegia, may recover miraculously

    49. However, evidence supports urgent decompression of bilateral locked facets in patients with incomplete tetraplegia or with neurologic deterioration.

      immediate decompression of bilateral locked facets in tetraplegic or deteriorating neurologicaly is suggested

    50. Historically, methylprednisolone was administered to patients with acute spinal cord injury after blunt injury, with clinical data suggesting a small benefit to initiating a 24-hour infusion if started within 3 hours and a 48-hour infusion if started within 3 to 8 hours.87 Current guidelines, however, no longer recommend steroids for acute injuries.

      methylprednisolone for acute spinal inj of blunt trauma for 24h infusion (if started in 3h) and 48h (if started in 3-8h) is no longer recommended

    51. Indications for immediate operative intervention are deterioration in neurologic function and fractures or dislocations with incomplete deficit

      neurologic deterioration and fx-dislocation with partial deficit indicate immediate op-intervention

    52. Surgical fusion typically is performed in patients with neurologic deficit, those with angulation of >11° or translation of >3.5 mm, and those who remain unstable after halo placement

      angulations of >11, translocation of >3.5mm, neuro-deficit, and post stabilizing unstability are candidates for fusion

    53. Immobilization of injuries also is achieved with spinal orthoses (braces), particularly in those with associated thoracolumbar injuries.

      spinal orthoses are also used especially thoracolumbar inj.

    54. In general, physician-supervised axial traction, via cervical tongs or the more commonly used halo vest, is used to reduce subluxations and stabilize the injury.

      halo vest or cervical tongs are used to stabilize ond decrease sublax via axial traction

    55. After initial stabilization, a systematic physical examination of the head and neck should be performed that also includes cranial nerve examination and three-dimensional CT scanning of the maxillofacial complex

      systematic PE of head-neck like CN exam and maxillofacial 3d CT should be considered after initial stabilization

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  2. onlinelibrary.wiley.com onlinelibrary.wiley.com
    1. In the epicenter of the current Italian epidemic, sudden cardiac death (SCD) likely occurred in many non-hospitalized patients with mild symptoms who were found dead home while in quarantine.
    2. Even after hospital discharge, we should consider that myocardial injury might result in atrial or ventricular fibrosis, the substrate for subsequent cardiac arrhythmias
    1. However, a recent pathological study found scarce interstitial mononuclear inflammatory infiltrates in heart tissue without substantial myocardial damage in a patient with COVID-19,13 suggesting that COVID-19 might not directly impair the heart.
    2. ompared with patients without cardiac injury, patients with cardiac injury presented with more severe acute illness, manifested by abnormal laboratory and radiographic findings, such as higher levels of C-reactive protein, NT-proBNP, and creatinine levels; more multiple mottling and ground-glass opacity; and a greater proportion requiring noninvasive or invasive ventilation.
    3. Consistently, our study also found 19.7% of patients with cardiac injury and first demonstrated that cardiac injury was independently associated with an increased risk of mortality in patients with COVID-19.
    4. After adjusting for age, preexisting cardiovascular diseases (hypertension, coronary heart disease, and chronic heart failure), cerebrovascular diseases, diabetes mellitus, chronic obstructive pulmonary disease, renal failure, cancer, ARDS, creatinine levels greater than 133 μmol/L, and NT-proBNP levels greater than 900 pg/mL, the multivariable adjusted Cox proportional hazard regression model showed a significantly higher risk of death in patients with cardiac injury than in those without cardiac injury, either during time from symptom onset (hazard ratio [HR], 4.26 [95% CI, 1.92-9.49]) or time from admission to study end point (HR, 3.41 [95% CI, 1.62-7.16]) (Table 3).
    5. The mortality rate was higher among patients with vs without cardiac injury (42 [51.2%] vs 15 [4.5%]; P < .001) as shown in Table 2 and the Kaplan-Meier survival curves in Figure 2. The mortality rate increased in association with the magnitude of the reference value of hs-TNI
    6. Patients with cardiac injury vs those without cardiac injury had shorter durations from symptom onset to follow-up (mean, 15.6 [range, 1-37] days vs 16.9 [range, 3-37] days; P = .001) and admission to follow-up (6.3 [range, 1-16] days vs 7.8 [range, 1-23] days; P = .039).
    7. Of patients with cardiac injury, only 22 (26.8%) underwent examination of electrocardiogram (ECG) after admission, and 14 of 22 ECGs (63.6%) were performed during the periods of elevation of cardiac biomarkers. All 14 ECGs were abnormal, with findings compatible with myocardial ischemia, such T-wave depression and inversion, ST-segment depression, and Q waves. The ECG changes in 3 patients with representative cardiac injury are shown in eFigure 2 in the
    8. In terms of radiologic findings, bilateral pneumonia (75 of 82 patients [91.5%] vs 236 of 334 patients [70.7%]) and multiple mottling and ground-glass opacity (53 [64.6%] vs 15 [4.5%]) were more prevalent in patients with than those without cardiac injury (both P < .001, Table 1).
    9. The duration of hospitalization before testing was longer in patients with cardiac injury than those without cardiac injury (median [range] time, 3 [1-15] days vs 2 [1-8] days; P < .001).
    10. The laboratory and radiologic findings are shown in Table 1. In the overall study population of 416 patients, median (IQR) levels of C-reactive protein (4.5 [1.4-8.5] mg/dL; to convert to milligrams per liter, multiply by 10) and procalcitonin (0.07 [0.04-0.15] ng/L) were elevated, while the median values of other laboratory indicators were within the normal range, such as counts of leukocytes, lymphocytes, platelets, erythrocytes; hemoglobin level; cardiac indicators
    11. In the present study, we also found that markers of inflammatory response, such as C-reactive protein, procalcitonin, and leukocytes, were significantly increased among patients who suffered from cardiac injury. The activation or enhanced release of these inflammatory cytokines can lead to apoptosis or necrosis of myocardial cells.
    12. Thus, because of the current limited evidence, the question of whether the SARS-CoV-2 virus can directly injure the heart requires further demonstration.
    13. In terms of laboratory findings, patients with cardiac injury compared with patients without cardiac injury showed higher median leukocyte count (median [IQR], 9400 [6900-13 800] cells/μL vs 5500 [4200-7400] cells/μL), and levels of C-reactive protein (median [IQR], 10.2 [6.4-17.0] mg/dL vs 3.7 [1.0-7.3] mg/dL), procalcitonin (median [IQR], 0.27 [0.10-1.22] ng/mL vs 0.06 [0.03-0.10] ng/mL), CK-MB (median [IQR], 3.2 [1.8-6.2] ng/mL vs 0.9 [0.6-1.3] ng/mL), myohemoglobin (median [IQR], 128 [68-305] μg/L vs 39 [27-65] μg/L), hs-TNI (median [IQR], 0.19 [0.08-1.12] μg/L vs <0.006 [<0.006-0.009] μg/L), N-terminal pro-B-type natriuretic peptide (NT-proBNP) (median [IQR], 1689 [698-3327] pg/mL vs 139 [51-335] pg/mL),
    14. Greater proportions of patients with cardiac injury required noninvasive mechanical ventilation (38 of 82 [46.3%] vs 13 of 334 [3.9%]; P < .001) or invasive mechanical ventilation (18 of 82 [22.0%] vs 14 of 334 [4.2%]; P < .001) than those without cardiac injury.
    15. creatinine kinase–myocardial band (median [IQR], 3.2 [1.8-6.2] vs 0.9 [0.6-1.3] ng/mL)
    16. N-terminal pro-B-type natriuretic peptide (median [IQR], 1689 [698-3327] vs 139 [51-335] pg/mL)
    1. Moreover, hypoxemia caused by COVID-19 may bring about atrial fibrillation, which is the most common arrhythmia among elderly individuals, and atrial fibrillation could be refractory before the pulmonary function is improved.
    1. There were numerous differences in laboratory findings between patients admitted to the ICU and those not admitted to the ICU (Table 2), including higher white blood cell and neutrophil counts, as well as higher levels of D-dimer, creatine kinase, and creatine.
    2. Thirty-six patients (26.1%) were transferred to the intensive care unit (ICU) because of complications, including acute respiratory distress syndrome (22 [61.1%]), arrhythmia (16 [44.4%]), and shock (11 [30.6%]).
    3. Heart rate, respiratory rate, and mean arterial pressure did not differ between patients who received ICU care and patients who did not receive ICU care. These measures were recorded on day of hospital admission for all patients, then divided into those who were later admitted to the ICU or not.
    4. Common complications among the 138 patients included shock (12 [8.7%]), ARDS (27 [19.6%]), arrhythmia (23 [16.7%]), and acute cardiac injury (10 [7.2%]). Patients who received care in the ICU were more likely to have one of these complications than non-ICU patients.
    1. The mortality during hospitalization was 7.62% (8 of 105) for patients without underlying CVD and normal TnT levels,
    2. for those without underlying CVD but elevated TnT levels, and 69.44% (25 of 36) for those with underlying CVD and elevated TnTs.
    3. Plasma TnT levels demonstrated a high and significantly positive linear correlation with plasma high-sensitivity C-reactive protein levels (β = 0.530, P < .001) and N-terminal pro–brain natriuretic peptide (NT-proBNP) levels (β = 0.613, P < .001). Plasma TnT and NT-proBNP levels during hospitalization (median [interquartile range (IQR)], 0.307 [0.094-0.600]; 1902.00 [728.35-8100.00]) and impending death (median [IQR], 0.141 [0.058-0.860]; 5375 [1179.50-25695.25]) increased significantly compared with admission values (median [IQR], 0.0355 [0.015-0.102]; 796.90 [401.93-1742.25]) in patients who died (P = .001; P < .001), while no significant dynamic changes of TnT (median [IQR], 0.010 [0.007-0.019]; 0.013 [0.007-0.022]; 0.011 [0.007-0.016]) and NT-proBNP (median [IQR], 352.20 [174.70-636.70]; 433.80 [155.80-1272.60]; 145.40 [63.4-526.50]) was observed in survivors
    4. During hospitalization, patients with elevated TnT levels had more frequent malignant arrhythmias, and the use of glucocorticoid therapy (37 [71.2%] vs 69 [51.1%]) and mechanical ventilation (41 [59.6%] vs 14 [10.4%]) were higher compared with patients with normal TnT levels.
  3. www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
    1. that the levels of the last test of neutrophils (14/16, 87.5%), PCT (11/11, 100%), CRP (11/13, 84.6%), cTnI (7/9, 77.8%),
    1. In severe cases, COVID-19 may present as pneumonia, the acute respiratory distress syndrome (ARDS), with or without both distributive and cardiogenic shock, to which elderly populations with preexisting medical comorbidities are the most vulnerable
    1. No study has described the incidence of ST-segment elevation myocardial infarction in COVID-19, but it appears to be low. Similarly, the incidence of left ventricular systolic dysfunction, acute left ventricular failure and cardiogenic shock have also not been described.
    2. However, an elevation of high-sensitivity cardiac troponin I (cTnI) above 99th percentile upper reference limit is the most commonly used definition
    1. We describe the first case of acute cardiac injury directly linked to myocardial localization of severe acute respiratory syndrome coronavirus (SARS‐CoV‐2) in a 69‐year‐old patient with flu‐like symptoms rapidly degenerating into respiratory distress, hypotension, and cardiogenic shock.
    2. An intra‐aortic balloon pump (IABP) was placed on top of adrenaline (0.07 μg/kg/min), and noradrenaline (0.1 μg/kg/min) was added for worsening hypotension (systolic blood pressure: 80/67/60 mmHg).
    3. The first echocardiography showed a dilated left ventricle [left ventricular (LV) end‐diastolic diameter 56 mm], severe and diffuse LV hypokinesia (LV ejection fraction 34%). Three hours later, LV ejection fraction dropped to 25% and estimated cardiac index was 1.4 L/min/m2. Coronary angiography findings were unremarkable.
    4. Vice versa, we did not observe viral particles in cardiac myocytes and, therefore, we cannot infer on viral cardiotropism. Cardiac myocytes showed non‐specific damage that was mainly characterized by focal myofibrillar lysis. In addition, we did not observe cytopathic endothelia and small intramural vessel inflammation or thrombosis. Other cases are needed to confirm this observation.
    5. Cardiac myocytes showed non‐specific features consisting of focal myofibrillar lysis, and lipid droplets. We did not observe viral particles in myocytes and endothelia. Small intramural vessels were free from vasculitis and thrombosis. EMB did not show significant myocyte hypertrophy or nuclear changes; interstitial fibrosis was minimal, focal, and mainly perivascular
    6. The pathologic study showed low‐grade interstitial and endocardial inflammation (Figure 1A and 1B). Large (>20 μm), vacuolated, CD68‐positive macrophages were seen with immune‐light microscopy (Figure 1C and 1D); they were ultrastructurally characterized by cytopathy, with membrane damage and cytoplasmic vacuoles (Figure 1E). The ultrastructural study demonstrated single or small groups of viral particles with the morphology (dense round viral envelope and electron‐dense spike‐like structures on their surface) and size (variable between 70 and 120 nm) of coronaviruses (Figure 2). COVID‐19 infected Vero cells were used as control. The viral particles were observed in cytopathic, structurally damaged interstitial cells that demonstrated loss of the cytoplasmic membrane integrity (Figure 3)
    1. By the end of Jan 25, 31 (31%) patients had been discharged and 11 (11%) patients had died; all other patients were still in hospital (table 1). The first two deaths were a 61-year-old man (patient 1) and a 69-year-old man (patient 2). They had no previous chronic underlying disease but had a long history of smoking.
    1. The clinical effects of pneumonia have been linked to increased risk of cardiovascular disease up to 10-year follow-up16 and it is likely that cases infected via respiratory virus outbreaks will experience similar adverse outcomes. Therapeutic use of corticosteroids further augments the possibility of adverse cardiovascular events. However, long-term follow-up data concerning the survivors of respiratory virus epidemics are scarce. Lipid metabolism remained disrupted 12 years after clinical recovery in a metabolomic study amongst 25 SARS survivors,17 whereas cardiac abnormalities observed during hospitalisation in eight patients with H7N9 influenza returned to normal at 1-year follow-up.
    1. The final diagnosis was acute virus-negative lymphocytic myocarditis associated with SARS-CoV-2 respiratory infection
    2. EMB (Panel E, day 7) documented diffuse T-lymphocytic inflammatory infiltrates (CD3+ >7/mm2) with huge interstitial oedema and limited foci of necrosis. No replacement fibrosis was detected, suggesting an acute inflammatory process. Molecular analysis showed absence of the SARS-CoV-2 genome within the myocardium. No contraction band necrosis or TTS-associated microvascular abnormalities were observed.
    3. CMR (day 7) showed a recovery of systolic function (from 52% by CTA to 64% by CMR), although with persistence of a mild hypokinesia at basal and mid left ventricular segments; at the same sites, diffuse myocardial oedema, determining wall pseudo-hypertrophy, was observed on short T1 inversion recovery (STIR) sequences (Panel D) and confirmed by T1 and T2 mapping (average native T1 = 1188 ms, normal value <1045; average T2 = 61 ms, normal value <50). Late gadolinium enhancement sequences demonstrated absence of detectable myocardial scar/necrotic foci.
    4. Although the first clinical suspicion was myocarditis, coronary computed tomography angiography (CTA) was acquired to rule out coronary artery disease (CAD). Baseline chest scan (Panel B) confirmed bilateral patchy ground-glass opacities; CTA showed no aortic dissection, pulmonary embolism, or epicardial CAD (Panel C). Dynamic 3D volume-rendering reconstruction demonstrated a clear hypokinesia of the left ventricle mid and basal segments, with normal apical contraction, suggesting a reverse Tako-Tsubo syndrome (TTS) pattern
    5. ECG (Panel A) showed low atrial ectopic rhythm, mild ST-segment elevation in leads V1–V2 and aVR, reciprocal ST depression in V4–V6, and QTc 452 ms with diffuse U-waves. The high-sensitivity troponin T curve was 135–107–106 ng/L (normal value <14), NT-proBNP 512 pg/mL (normal value <153), and C-reactive protein 18 mg/L (normal value <6). Transthoracic echocardiogram showed mild left ventricular systolic dysfunction (LVEF 43%) with inferolateral wall hypokynesis; neither ventricle was dilated and there was no pericardial effusion.
    1. Itis likely that cardiac troponin measurements wererequested in those who were more unwell or where there wasreasonable suspicion of myocardial ischemia or myocardial dysfunction. Only systematic testing of both symptomatic and asymptomatic patients infected with SARS-CoV-2 will provide an accurate estimate of the prevalence of myocardial injuryin this condition.
    2. In a cohort of 191 patients with confirmed COVID-19 based on SARS-CoV-2 RNA detection, the univariable odds ratio for death when hs-cTnI concentrations were above the 99thpercentile upper reference limit was 80.1 (95% confidence interval [CI]10.3 to 620.4, P<0.0001).[4]This was higher than the odds ratios observed for all other biomarkerstested,including D-Dimer and lymphocyte count.
    1. While the spectrum of clinical manifestation is highly related to the inflammation process of the respiratory tract, this case provides evidence of cardiac involvement as a possible late phenomenon of the viral respiratory infection. This process can be subclinical with few interstitial inflammatory cells, as reported by an autopsy study,10 or can present with overt manifestations even without respiratory symptoms, as in the present case.
    2. A 12-lead electrocardiogram (ECG) showed low voltage in the limb leads, minimal diffuse ST-segment elevation (more prominent in the inferior and lateral leads), and an ST-segment depression with T-wave inversion in lead V1 and aVR
    3. Chest radiography was repeated on day 4 and showed no thoracic abnormalities. Transthoracic echocardiography, performed on day 6, revealed a significant reduction of LV wall thickness (interventricular septum, 11 mm; posterior wall, 10 mm), an improvement of LVEF to 44%, and a slight decrease of pericardial effusion (maximum, 8-9 mm). At the time of submission, the patient was hospitalized with progressive clinical and hemodynamic improvement.
    4. During the first days of her hospitalization, the patient remained hypotensive (systolic blood pressure less than 90 mm Hg) and required inotropic support (dobutamine) in the first 48 hours, during which there was a further increase in levels of NT-proBNP (8465 pg/mL), high-sensitivity troponin T (0.59 ng/mL), and creatine kinase–MB (39.9 ng/mL), with a progressive stabilization and reduction during the following days (Table). Blood pressure progressively stabilized, although systolic pressure remained less than 100 mm Hg, and dobutamine treatment was weaned on day 4.
    5. Transthoracic echocardiography revealed normal left ventricular (LV) dimensions with an increased wall thickness (interventricular septum, 14 mm, posterior wall, 14 mm) and a diffuse echo-bright appearance of the myocardium. There was diffuse hypokinesis, with an estimated LV ejection fraction (LVEF) of 40%. There was no evidence of heart valve disease. Left ventricular diastolic function was mildly impaired with mitral inflow patterns, with an E/A ratio of 0.7 and an average E/e′ ratio of 12. There was a circumferential pericardial effusion that was most notable around the right cardiac chambers (maximum, 11 mm) without signs of tamponade. Cardiac magnetic resonance imaging (MRI) confirmed the increased wall thickness with diffuse biventricular hypokinesis, especially in the apical segments, and severe LV dysfunction (LVEF of 35%) (Video 1 and Video 2). Short tau inversion recovery and T2-mapping sequences showed marked biventricular myocardial interstitial edema. Phase-sensitive inversion recovery sequences showed diffuse late gadolinium enhancement extended to the entire biventricular wall (Figure 2). The myocardial edema and pattern of late gadolinium enhancement fulfilled all the Lake Louise criteria for the diagnosis of acute myocarditis.6 The circumferential pericardial effusion was confirmed, especially around the right cardiac chambers (maximum, 12 mm).
    6. Cardiac magnetic resonance imaging showed increased wall thickness with diffuse biventricular hypokinesis, especially in the apical segments, and severe left ventricular dysfunction (left ventricular ejection fraction of 35%). Short tau inversion recovery and T2-mapping sequences showed marked biventricular myocardial interstitial edema, and there was also diffuse late gadolinium enhancement involving the entire biventricular wall. There was a circumferential pericardial effusion that was most notable around the right cardiac chambers. These findings were all consistent with acute myopericarditis.
    1. In addition, repeated floods of catecholamines due to anxiety and the side effects of medication can also lead to myocardial damage.
    2. Third, Huang’s study noted that high concentration of IL-1β, IFN-γ, IP-10 and MCP-1 could be detected in patients infected with 2019-nCoV, which might lead to activated T-helper-1 (Th1) cell responses [4]. Furthermore, they also found that ICU patients had much higher concentrations of inflammatory factors than those non-ICU patients, suggesting that the cytokine storm was associated with disease severity
    3. Second, hypoxaemia may be also an important reason of cardiac injury. In Huang’s study, 32% COVID-19 patients had various degree of hypoxaemia and need required high-flow nasal cannula or higher-level oxygen support. In Chen’s study, up to 76% of patients require oxygen therapy. Due to severe 2019-nCoV infection, the pneumonia may cause significant gas exchange obstruction, leading to hypoxaemia, which significantly reduces the energy supply by cell metabolism, and increases anaerobic fermentation, causing intracellular acidosis and oxygen free radicals to destroy the phospholipid layer of cell membrane. Meanwhile, hypoxia-induced influx of calcium ions also leads to injury and apoptosis of cardiomyocytes.
    4. The data again showed a significant higher incidence of acute cardiac injury in ICU/severe patients compared to the non-ICU/severe patients [RR = 13.48, 95% CI (3.60, 50.47), Z = 3.86, P = 0.0001]
    5. Another two studies only gave the data of creatine kinase, if it can be seen as a biomarker of cardiac injury, the proportion might be 11.5% (95% CI 7.8–15.2%).
    6. Two studies that gave clear data were statistically analyzed, and the data showed that 8.0% (95% CI 4.1–12.0%) patients might be suffered from an acute cardiac injury.
    1. It is reasonable to expect that severe and critical cases have more severe effects on the cardiovascular system owing to more robust inflammatory response. At this early stage, our knowledge is mainly based on available numerators data, and the exact population-level denominators are not known. Also, it is likely that the asymptomatic and mildly symptomatic cases are missing from most reports, which further skews our understanding of the disease.
    1. There were no obvious histological changes seen in heart tissue, suggesting that SARS-CoV-2 infection might not directly impair the heart
    2. There were a few interstitial mononuclear inflammatory infiltrates, but no other substantial damage in the heart tissue
    1. Based on the analysis of the clinical data, we confirmed that some patients died of fulminant myocarditis. In this study, we first reported that the infection of SARS-CoV-2 may cause fulminant myocarditis.
    2. Among the 68 fatal cases, 36 patients (53%) died of respiratory failure, five patients (7%) with myocardial damage died of circulatory failure, 22 patients (33%) died of both, and five remaining died of an unknown cause
    1. Among survivors, secondary infection, acute kidney injury, and acute cardiac injury were observed in one patient each, occurring 9 days (acute kidney injury), 14 days (secondary infection), and 21 days (acute cardiac injury) after illness onset.
    2. Creatine kinase, U/L≤1851 (ref)......>1852·56 (1·03–6·36)0·043....High-sensitivity cardiac troponin I, pg/mL≤281 (ref)......>2880·07 (10·34–620·36)<0·0001....
    3. In this study, increased high-sensitivity cardiac troponin I during hospitalisation was found in more than half of those who died.
    4. Heart failure44 (23%)28 (52%)16 (12%)<0·0001Septic shock38 (20%)38 (70%)0<0·0001Coagulopathy37 (19%)27 (50%)10 (7%)<0·0001Acute cardiac injury33 (17%)32 (59%)1 (1%)<0·0001Acute kidney injury28 (15%)27 (50%)1 (1%)<0·0001
    1. COVID‐19 prognosis is related to age and sex. The expression of ACE2 decreases with increasing age. ACE2 expression is higher in young people than in elderly individuals and higher in females than in males.11, 12 This pattern does not match the characteristic of severely ill COVID‐19 patients being mostly elderly males. We believe that whether the level of ACE2 expression is high or low is not a key factor affecting the prognosis of patients with COVID‐19. The relationship between sex and prognosis requires additional data to verify.

      some believe that ACe2 level of expression does not correlate covid-19 prognosis

    1. Duration from onset of symptoms to radiological confirmation of pneumonia, days5 (3–9)5 (3–7)Duration from onset of symptoms to ICU admission, days9 (6–12)11 (7–14)Heart rate, beats per min89 (20)89 (15)Systolic blood pressure, mm Hg133 (20)140 (21)
    2. Cardiac injury3 (15%)9 (28%)12 (23%)
    3. By Jan 26, 2020, 710 patients had been admitted to Wuhan Jin Yin-tan hospital with confirmed SARS-CoV-2 pneumonia, of whom 658 (93%) were considered ineligible, including three patients who had cardiac arrest immediately after admission.
    1. A raised troponin (hypersensitive-troponin I (hs-cTnI)) was detected in five patients, possibly suggestive of virus-associated myocardial injury.
    1. Despite low expression in CMs, ACE2 was highly and specifically expressed in pericytes (Figure 1E). In addition, the expression of ABCC9 and PDGFRB and the absence of MYH11 help us to reaffirm the identity of the cells as pericytes instead of SMCs (Figure 1F). Different from SMCs that are located in the coronary arteries or arterioles, pericytes spread outside the endothelial cell of capillary and part of venules, which may play an essential role in myocardial micro-circulation. This result suggested that pericyte was a potential SARS-CoV-2 virus targeted host cell type in the human heart. We further screened another two related receptors of SARS-CoV, CD209, and CLEC4M. CD209 was specifically expressed in macrophage, and co-expressed with macrophage marker gene CD163, which may enhance the virus entry in the human heart (Figure 1G). CLEC4M was not enriched in human heart cells.
    1. Lewis male rats, 166 we found that the ARB losartan increased ACE2 activity in the heart by 2 to 3-fold as
    2. experimental studies reveal that statins also augment the ACE2 198 expression. Tikoo et al. (45)
    1. Northern blot analysis revealed a ≈3.4-kb ACE2 transcript expressed only in heart, kidney, and testis of 23 human tissues examined; a minor ≈8-kb band was also detected in kidney
    1. When Ace2 is transgenically overexpressed in mouse heart, cardiac defects are again observed, most notably a lethal ventricular arrhythmia, which is associated with disruption of gap junction formation [9Donoghue M et al.Heart block, ventricular tachycardia, and sudden death in ACE2 transgenic mice with downregulated connexins.J. Mol. Cell. Cardiol. 2003; 35: 1043-1053Abstract Full Text Full Text PDF PubMed Scopus (142) Google Scholar]. The high incidence of sudden death in these mice correlated with the levels of Ace2 transgene expression. Surviving older mice showed a spontaneous downregulation of the transgene and restoration of normal cardiac function.
    1. The mechanism of acute myocardial injury caused by SARS-CoV-2 infection might be related to ACE2. ACE2 is widely expressed not only in the lungs but also in the cardiovascular system and, therefore, ACE2-related signalling pathways might also have a role in heart injury.
    2. Other proposed mechanisms of myocardial injury include a cytokine storm triggered by an imbalanced response by type 1 and type 2 T helper cells
    3. Among the people who died from COVID-19 reported by the NHC, 11.8% of patients without underlying CVD had substantial heart damage, with elevated levels of cTnI or cardiac arrest during hospitalization.
    4. and respiratory dysfunction and hypoxaemia caused by COVID-19, resulting in damage to myocardial cells.
    5. some of the patients first went to see a doctor because of cardiovascular symptoms. The patients presented with heart palpitations and chest tightness rather than with respiratory symptoms, such as fever and cough, but were later diagnosed with COVID-19.
    1. Of the 305 patients, 146 were male (47.9%) and 159 were female (52.1%); the median age was 57 years old; 84.1% (228/271) had a positive nasopharyngeal swab or pharyngeal swab nucleic acid test; dangerous recombination 46 cases (15.1%) and 259 non-risk reorganizations (84.9%). The incubation period is 1 to 15 days, and the median period is 6 days. The initial symptoms were mainly fever, cough, fatigue, and decreased appetite, accounting for 81.1% (163/201), 39.3% (79/201), 54.7% (110/201), and 50.2% (101/201). 79.1% (159/201) patients had gastrointestinal symptoms 1 to 10 days after the onset, including nausea 29.4% (59/201), vomiting 15.9% (32/201), abdominal pain 6.0% (12/201) . 49.5% (146/295) patients had diarrhea, with a median time of 3.3 days, (3.3 ± 1.6) times / day, and sustained (4.1 ± 2.5) days; excluding possible drug-related diarrhea, the incidence of diarrhea was still 22.2 %, But only 6.9% (4/58) of patients routinely found positive leukocytes or fecal occult blood. 39.1% (119/304) patients had elevated ALT, AST or bilirubin upon admission, of which ALT, AST ≥80 U / L accounted for only 7.9% (24/304) and 6.3% (19/304); Only 2.0% (6/304) had bilirubin elevation, and the average level was (37.4 ± 21.1) μmol / L. The median age of risky reorganization is greater than that of non-risk reorganization (65.5 years to 56 years old, P <0.05), the proportion of patients with abnormal liver function upon admission [67.4% (31/46) vs. 34.1% (88/258)], mild AST The proportion of people with elevated (40-80 U / L) [47.8% (22/46) vs.

      Fontaine et al in a retrospective analysis of new-type coronavirus pneumopnia (NCP) found 79.1% (159/201) patients with incubation period is 1 to 15 days, had initial GI related symptoms from 1 to 10 days after onset, including nausea 29.4% (59/201), vomiting 15.9% (32/201), abdominal pain 6.0% (12/201). plus decreased appetite 50.2% (101/201) which was not counted as GI presentation. 49.5% 146/295) patients had diarrhea, with a median time of 3.3 days, (3.3 ± 1.6) times / day, and sustained (4.1 ± 2.5) days, excluding possible drug-related diarrhea the insidence was still 22.2%, 6.9% (4/58) of patients found to have leukocytes or fecal occult blood.

    1. Indications for operative treatment of thoracic injuries Initial tube thoracostomy drainage of >1000 mL (penetrating injury) or >1500 mL (blunt injury) Ongoing tube thoracostomy drainage of >200 mL/h for 3 consecutive hours in noncoagulopathic patients Caked hemothorax despite placement of two chest tubes Great vessel injury (endovascular techniques may be used in selected patients) Pericardial tamponade Cardiac herniation Massive air leak from the chest tube with inadequate ventilation Tracheal or main stem bronchial injury diagnosed by endoscopy or imaging Open pneumothorax Esophageal perforation Air embolism

      1000ml drainage (penetrating), >1500mlm (blunt) from tube. >200mL/h for 3h nonstop drainage in noncoagulopathic px. caked hemothorax after two chest tubes.great vessels inj. pericardial tamp. hernia of heart. inadequate ventilation with massive air leak.main stem or tracheal damage (imaginf or endoscopy). open pneumothorax. perforation of esophagus. air embolism